【摘要】 目的:探讨丝裂素活化蛋白激酶在血管紧张素Ⅱ(AngⅡ)诱导血管平滑肌细胞(VSMC)转化生长因子-β受体(TGF-βR1)上调中的作用。方法:培养大鼠主动脉VSMC,以10-7mol/L AngⅡ刺激作为AngⅡ组,AngⅡ刺激前分别应用10-5mol/L氯沙坦(Losartan)、PD98059预处理,以正常的VSMC为对照组,细胞免疫化学法测定培养12h时VSMC TGF-βR1的含量。结果:与对照组相比,AngⅡ刺激培养12h的VSMC TGF-βR1表达上调(P<0.01);AngⅡ受体AT1型拮抗剂Losartan使TGF-βR1表达显著降低(P<0.01),丝裂素活化蛋白激酶抑制剂PD98059能显著降低TGF-βR1表达(P<0.05)。结论:AngⅡ通过AT1上调TGF-βR1的表达,丝裂原活化蛋白激酶参与AngⅡ的胞内信号转导。更多还原

【Abstract】 Objective:To study the role of mitogen activated protein kinase in up-regulation of transforming growth factor receptor induced by angiotensin Ⅱ in vascular smooth muscle cell in rats in vitro. Methods:The cultured VSMCs were Pretreated with 10-7mol/L AngⅡ as AngⅡ group, the cultured VSMC pretreated with Losartan, PD98059 with 10-7mol/L AngⅡ, the normol cultured VSMC as control group. TGF-βR1 was detected by immunocytochemical technique. Results :TGF-βR1 expression in AngⅡ group was higher than that in control(P <0.01),pretreated with Losartan, PD98059, TGF-β R1 expression were obviously lower than that in AngⅡ group(P<0.01, P <0.05,respectively). Conclusion :TGF-β R expression can be up-regulated by Ang Ⅱ through the AT1 receptor and the pathway is involved in by mitogen activated protein kinase.更多还原